ArticleJournal of neurotrauma2013
Cerebral glucose metabolism in an immature rat model of pediatric traumatic brain injury.
Article in Journal of neurotrauma, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 30 citations in OpenAlex.
- NMR metabolomics in genetically engineered mouse models.Biophysical reviews · 2025Review
- Metabolic Imaging of Hyperpolarized [1-International journal of molecular sciences · 2025Article
- Tracing the path of disruption:CNS neuroscience & therapeutics · 2024Review
- Exploring the Role of SMPD3 in the lncRNA-miRNA-mRNA Regulatory Network in TBI Progression by Influencing Energy Metabolism.Journal of inflammation research · 2024Article
- Early metabolic derangements and unfavorable outcomes in pediatric traumatic brain injury: a retrospective multi-center cohort study.Translational pediatrics · 2023Article
- Reactive oxygen species-responsive HET0016 prodrug-loaded liposomes attenuate neuroinflammation and improve neurological deficit in a rat model of juvenile traumatic brain injury.Frontiers in neuroscience · 2023Article
- Metabolism of Exogenous [2,4-Metabolites · 2022Article
- Traumatic brain injury metabolome and mitochondrial impact after early stage Ru360 treatment.Mitochondrion · 2021Article
- Kaempferol Treatment after Traumatic Brain Injury during Early Development Mitigates Brain Parenchymal Microstructure and Neural Functional Connectivity Deterioration at Adolescence.Journal of neurotrauma · 2020Article
- Bridging the gap: Mechanisms of plasticity and repair after pediatric TBI.Experimental neurology · 2019Review
- Metabolic perturbations after pediatric TBI: It's not just about glucose.Experimental neurology · 2019Review
- Beneficial Effects of Kaempferol after Developmental Traumatic Brain Injury Is through Protection of Mitochondrial Function, Oxidative Metabolism, and Neural Viability.Journal of neurotrauma · 2019Article
- Consolidated Biochemical Profile of Subacute Stage Traumatic Brain Injury in Early Development.Frontiers in neuroscience · 2019Article
- Early behavioral and metabolomic change after mild to moderate traumatic brain injury in the developing brain.Neurochemistry international · 2018Article
- Scaled traumatic brain injury results in unique metabolomic signatures between gray matter, white matter, and serum in a piglet model.PloS one · 2018Article
- Glucose metabolism in pediatric traumatic brain injury.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2017Review
- Glucose and Intermediary Metabolism and Astrocyte-Neuron Interactions Following Neonatal Hypoxia-Ischemia in Rat.Neurochemical research · 2017Review
- Serum Metabolic Profiling Reveals Altered Metabolic Pathways in Patients with Post-traumatic Cognitive Impairments.Scientific reports · 2016Article
- Neuronal Cell Death Induced by Mechanical Percussion Trauma in Cultured Neurons is not Preceded by Alterations in Glucose, Lactate and Glutamine Metabolism.Neurochemical research · 2016Article
- The Controlled Cortical Impact Model: Applications, Considerations for Researchers, and Future Directions.Frontiers in neurology · 2016Review
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Altered cerebral metabolism and mitochondrial function have been identified in experimental and clinical studies of pediatric traumatic brain injury (TBI). Metabolic changes detected using (1)H (proton) magnetic resonance spectroscopy correlate with long-term outcomes in children after severe TBI. We previously identified early (4-h) and sustained (24-h and 7-day) abnormalities in brain metabolites after controlled cortical impact (CCI) in immature rats. The current study aimed to identify specific alterations of cerebral glucose metabolism at 24 h after TBI in immature rats. Rats (postnatal days 16-18) underwent CCI to the left parietal cortex. Sham rats underwent craniotomy only. Twenty-four hours after CCI, rats were injected (intraperitoneally) with [1,6-(13)C]glucose. Brains were removed, separated into hemispheres, and frozen. Metabolites were extracted with perchloric acid and analyzed using (1)H and (13)C-nuclear magnetic resonance spectroscopy. TBI resulted in decreases in N-acetylaspartate in both hemispheres, compared to sham contralateral. At 24 h after TBI, there was significant decrease in the incorporation of (13)C label into [3-(13)C]glutamate and [2-(13)C]glutamate in the injured brain. There were no differences in percent enrichment of [3-(13)C]glutamate, [4-(13)C]glutamate, [3-(13)C]glutamine, or [4-(13)C]glutamine. There was significantly lower percent enrichment of [2-(13)C]glutamate in both TBI sides and the sham craniotomy side, compared to sham contralateral. No differences were detected in enrichment of (13)C glucose label in [2-(13)C]glutamine, [2-(13)C]GABA (gamma-aminobutyric acid), [3-(13)C]GABA, or [4-(13)C]GABA, [3-(13)C]lactate, or [3-(13)C]alanine between groups. Results suggest that overall oxidative glucose metabolism in the immature brain recovers at 24 h after TBI. Specific reductions in [2-(13)C]glutamate could be the result of impairments in either neuronal or astrocytic metabolism. Future studies should aim to identify pathways leading to decreased metabolism and develop cell-selective "metabolic rescue."
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